hi the following info stood out for me, one because i do so much reading about nutrition, and two because you mentioned something about hubby's physically demanding job:
http://www.mayoclinic.com/health/periph ... DSECTION=4
"Your risk of developing peripheral neuropathy is also higher if you have one or more of the following risk factors:
Excessive drinking of alcohol can affect your nervous system, causing numbness of your hands and feet.
A lack of certain vitamins, especially B-1 (thiamin) and B-12 makes peripheral neuropathy more likely. Pernicious anemia, which occurs when your body can't absorb B-12 properly, often leads to peripheral neuropathy.
Immune system disorders.
You're more likely to develop peripheral neuropathy if you have an autoimmune disease, such as lupus or rheumatoid arthritis, or if your immune system is compromised by the human immunodeficiency virus (HIV) or AIDS.
Other health problems.
Medical conditions, including certain types of cancer, kidney disease and liver disease, also can put you at risk of nerve damage.
A job or hobby that puts stress on one nerve for long periods of time increases your chances of developing peripheral neuropathy. In carpal tunnel syndrome, for example, the median nerve that extends through your wrist into your fingers becomes compressed. Repetitive assembly line work or work involving prolonged, heavy gripping can compress the median nerve. Playing golf, tennis or a musical instrument and using vibrating power tools or even crutches also can put pressure on peripheral nerves.
Exposure to some toxic substances can make you susceptible to peripheral nerve damage. These substances include heavy metals, such as lead, mercury and arsenic; organic solvents; and certain medications, such as those used to treat cancer or AIDS.
also, here are two interesting studies i found on a cuban epidemic of peripheral neuropathy - i like that it highlights the importance of nutrition and also that it shows optic neuropathy in a peripheral/toxin/nutrient context.
J Neurol Sci. 1994 Dec 1;127(1):11-28.
An epidemic in Cuba of optic neuropathy, sensorineural deafness, peripheral sensory neuropathy and dorsolateral myeloneuropathy.
Neuroepidemiology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
An epidemic outbreak of peripheral neuropathy affected Cuba in 1992-93 resulting in 50,862 cases (national cumulative incidence rate (CIR) 461.4 per 100,000). Clinical forms included retrobulbar optic neuropathy, sensory and dysautonomic peripheral neuropathy, dorsolateral myeloneuropathy, sensorineural deafness, dysphonia and dysphagia, spastic paraparesis, and mixed forms. For epidemiological purposes, cases were classified as optic forms (CIR 242.39) or peripheral forms (CIR 219.25). Increased risk was found among smokers (odds ratio (OR) 4.9), those with history of missing meals (OR 4.7) resulting in lower intake of animal protein, fat, and foods that contain B-vitamins, combined drinking and smoking (OR 3.5), weight loss (OR 2.
, excessive sugar consumption (OR 2.7) and heavy drinking (OR 2.3). Optic neuropathy was characterized by decreased vision, bilateral and symmetric central or cecocentral scotomata, and loss of color vision due to selective lesion of the maculopapillary bundles. Peripheral neuropathy was a distal axonopathy lesion affecting predominantly large myelinated axons. Deafness produced selective high frequency (4-8 kHz) hearing loss. Myelopathy lesions combined dorsal column deficits and pyramidal involvement of lower limbs with spastic bladder. Clinical features were those of Strachan syndrome and beriberi. Intensive search for neurotoxic agents, in particular organophosphorus esters, chronic cyanide, and trichloroethylene intoxication, yielded negative results. Treatment of patients with B-group vitamins and folate produced rewarding results. Most patients improved significantly and less than 0.1% of them remained with sequelae; there were no fatal cases. Supplementation of multivitamins to the entire Cuban population resulted in curbing of the epidemic. Overt malnutrition was not present, but a deficit of micronutrients, in particular thiamine, cobalamine, folate and sulfur amino acids appears to have been a primary determinant of this epidemic.
Rev Neurol. 1997 Dec;25(148):1848-52.
Rev Neurol. 1998 May;26(153):840.
[Clinical characteristics of Cuban epidemic neuropathy]
Gomez-Viera N, Rodriguez-Silva H, Perez-Nellar J, Telleria-Diaz A, Nassiff A, Marquez M, Caceres M, Rivero-Arias E.
Hospital Clinico Quirurgico Hermanos Ameijeiras, La Habana, Cuba.
INTRODUCTION: At the beginning of 1992 an epidemic neuropathy was seen in Cuba. MATERIAL AND METHODS: To determine the clinical characteristics we studied the clinical and neurological features, cerebrospinal fluid, and did neurophysiological investigations and sural nerve biopsies. RESULTS: Sixty patients were studied. Of these, 42 (70%) had polyneuropathy which was predominantly peripheral and 18 (30%) had combined forms. Most patients had asthenia and weight loss. The polyneuropathic effects were mainly in the legs. In 33.3% of the patients there were distal autonomic effects and sphincter disorders. Only 7 patients had hypoacusia. However, subclinical neurosensorial hypoacusia was seen in 33.3%. Optic neuropathy affected central vision bilaterally and symmetrically with temporal pallor of the papilla in half the cases. In 3 patients there was loss of ganglionar nerve fibres of the papillo-macula bundle. The contrast sensitivity visual test was abnormal in some patients with peripheral polyneuropathy, showing subclinical optic neuropathy in these cases. Sensory neuroconduction suggested axonal neuropathy in 30 patients, demyelinating neuropathy in 5 patients, while the remainder were normal. Motor neuroconduction was normal in most patients. Sural nerve biopsy of 27 patients showed axon damage in 96.2% of cases. CONCLUSIONS: The clinical picture is similar to that seen in nutritional deficiencies and toxic processes.